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Biomedical subjects

A Levy

Publications and source records attributed to A Levy.

At least 415 records · Page 23Linked to original sources
PubMed1984

Central vs peripheral anticholinergic effects on repeated acquisition of behavioral chains.

Monkeys that were required to repeatedly learn new sequences of responses to obtain food were injected with 0.2 mg/kg of atropine sulfate or methylatropine nitrate. Effects lasted 8 to 12 hr following injection. Both drugs decreased the rate at which the animals worked, but only atropine sulfate increased the number of attempts required to solve the problem and decreased overall accuracy, suggesting a peripheral mode of action for rate-decreasing effects, and a central mode of action for effects of atropine on qualitative aspects of performance.

Animals↗
PubMed1984

Dynamics of hemoglobin investigated by Mössbauer spectroscopy.

Mössbauer Spectra of Fe enriched horse hemoglobin and sperm whale myoglobin were measured in the temperature range from 80 K to 260 K. An analysis of the temperature dependence of the recoiless fraction (the Lamb-Mössbauer factor) shows it to be sensitive to conformational fluctuations which affect the mean square displacement of the iron. We have found that the protein conformation has a dramatic effect on these measurements. For hemoglobin greater conformational fluctuations at lower temperatures are observed for carbonmonoxyhemoglobin in the liganded conformation than for deoxyhemoglobin in the unliganded conformation. On the other hand, the Lamb-Mössbauer factor is insensitive to the binding of ligands to myoglobin and shows conformational fluctuations similar to deoxyhemoglobin even in the liganded state. It is also shown that a reversible complex with the distal histidine is formed in frozen deoxyhemoglobin solution above 200 K where the Lamb-Mössbauer factor shows the excitation of new modes of conformational fluctuations. This complex is not formed with carbonmonoxyhemoglobin which already has a sixth ligand and with deoxymyoglobin which appears to undergo much more limited conformational fluctuations. A possible relationship between the formation of the distal histidine complex and the cooperative ligand binding reaction is suggested by results with partially liganded hemoglobin which indicate increased formation of the distal histidine complex.

Animals↗
PubMed1984

Evidence for membrane-mediated chromosomal damage by aflatoxin B1 in human lymphocytes.

The hepatocarcinogen aflatoxin B1 (AFB1) was found to be a potent clastogen for phytohemagglutinin stimulated human lymphocytes. It also induced sister chromatid exchanges. These types of chromosomal damage were induced at very low levels of covalent AFB1 - DNA adducts suggesting that AFB1 operates in part by indirect action because of its membrane-active character. The membrane-active character of AFB1 is documented by the following results: (i) AFB1 stimulated the excretion of hydroxy- and/or hydroperoxy-arachidonic acid (AA) and free AA into the culture medium; (ii) the phospholipase A2 inhibitor p-bromophenacylbromide was anticlastogenic ; (iii) the inhibitors of the oxidative metabolism of AA indomethacin, flufenamic acid, 5,8,11,14-eicosatetraynoic acid, nordihydroguaiaretic acid and BN 1015 were anticlastogenic . These results are compatible with the induction of DNA damage by indirect action or the formation of covalent adducts via metabolic activation by cooxygenation . The observation that CuZn superoxide dismutase was anticlastogenic indicates the intermediacy of superoxide in DNA damage formation and supports the former mechanism.

Aflatoxin B1↗
PubMed1984

Ketoconazole--an effective treatment for disseminated pityriasis versicolor.

Long-standing disseminated lesions of pityriasis versicolor (PV) were found in 101 patients. As they had failed to respond to various topical agents, we treated them with 200 mg/day of ketoconazole. All of them were under clinical and mycological surveillance at weekly intervals. In successive mycological examinations during the course of therapy, an increased ratio of filaments/spores was observed, and the last positive examinations invariably showed the presence of only a few filaments and no spores. The mean duration of therapy, until a negative mycological smear was obtained, was 2.2 weeks. Side effects were insignificant, and did not necessitate interrupting treatment except in one patient, who developed an allergic eruption after a single 200-mg dose of the drug. The transient minor disturbances in liver function tests noted in six patients were considered drug related, but ketoconazole administration was continued in all these patients, and the values normalized gradually during treatment. We conclude that ketoconazole is a well-tolerated and highly effective drug in the systemic therapy of disseminated PV.

Administration, Oral↗
PubMed1983

Changes in chromatin structure at the replication fork. DNase I and trypsin-micrococcal nuclease effects on approximately 300- and 150-base pair nascent DNAs.

DNase I, trypsin, and micrococcal nuclease are used to further probe the structure of nascent deoxyribonucleoprotein (DNP) fractions which appear after in vivo 20-s pulse labeling of sea urchin embryos with [3H]thymidine. We present evidence that the large nascent DNP which protects the approximately 300-base pair large nascent DNA consists of at least one nucleosome core. This is based on fractionation in denaturing polyacrylamide gels of DNA extracted from large nascent DNP fractions of a micrococcal nuclease + DNase I digest of nuclei. The data also suggest the existence of a DNase I-hypersensitive site(s) within the large nascent DNP; this is consistent with the hypothesis that the latter consists of closely packed dinucleosome cores. Histone H1 and non-histone proteins do not account for the previously reported unusual hyperresistance of the large nascent DNA against micrococcal nuclease. The protection offered this approximately 300-base pair nascent DNA was not eliminated by an 0.2-microgram/ml trypsin pretreatment which removes the above proteins from the chromatin. However, 5-10 micrograms/ml of trypsin, which remove a portion of the NH2 termini of the four core histones of nucleosomes, eliminate the hyperresistance of the large nascent DNA to subsequent micrococcal nuclease digestion, while nascent and bulk monomer DNAs remain unaffected. This indicates histone-histone and/or histone-DNA interactions within the large nascent DNP which differ from those of nascent and bulk mononucleosome cores.

Animals↗
PubMed1983

Suppression of tumor promoter phorbolmyristate acetate-induced chromosome breakage by antioxidants and inhibitors of arachidonic acid metabolism.

To gain insight into the mechanism of formation of chromosomal aberrations by the tumor promoter phorbolmyristate acetate (PMA) in human lymphocytes, we investigated the effect of antioxidants and inhibitors of arachidonic acid metabolism. Among the antioxidants bovine erythrocyte CuZn superoxide dismutase, glutathione peroxidase, mannitol (a scavenger of hydroxyl radicals), butylated hydroxytoluene and butylated hydroxyanisole were anticlastogenic while catalase and dimethylfuran (a scavenger of singlet oxygen) were inactive. These results show that the induction of aberrations by PMA occurs via indirect action, i.e. the intermediacy of superoxide and hydroxyl radicals. The following inhibitors of arachidonic acid metabolism were strongly anticlastogenic: the cyclo-oxygenase inhibitors indomethacin and flufenamic acid and the lipoxygenase inhibitor BN1015. Imidazole, nordihydroguaiaretic acid BN1048 and 5,8,11,14-eicosatetraynoic acid were moderately active. The inhibitor of phospholipase A2, fluocinolone acetonide, was also anticlastogenic. We conclude that the oxidative metabolism of arachidonic acid is involved in the induction of chromosomal aberrations by PMA in human lymphocytes. However, because of the limited selectivity of these drugs, it is not yet possible to identify unambiguously the step(s) in the arachidonic acid cascade responsible for PMA clastogenicity.

Anti-Inflammatory Agents↗
PubMed1983

Alcohol-preferring rats in colonies show withdrawal, inactivity, and lowered dominance.

Rats with free access to water and 10% alcohol were raised in enriched, social colonies for prolonged periods of time. Then those animals which had developed extreme alcohol or water preferences were identified for further study. These selected animals were marked and returned to the colony. Both high and low alcohol consumers showed increased alcohol consumption just prior to feeding, but only the high consumers had a peak of alcohol consumption during the early morning hours. Compared to low consumers, high alcohol consumers ate less food, ran less in the activity wheel, spent more time in the burrows, and ranked low on several dominance measures. When access to alcohol was removed in the colony, these high alcohol consumers became more active but remained low in dominance. When tested in photocell cages, they showed a pattern of hyperactivity suggesting withdrawal effects. This sub-population of animals from rat colonies who voluntarily prefer alcohol to water represent a novel and social animal model of chronic alcohol consumption.

Alcohol Drinking↗